Neglect is a human clinical syndrome characterized by a failure to act in, or toward the hemispace contralateral to a lesion. The neglect syndrome can be extremely debilitating to the patient and family for a period of weeks to months. At present, the mechanisms of behavioral recovery from cortical neglect are unknown. The present proposed studies will provide a direct examination of the pharmacological basis of recovery from multimodal neglect produced by unilateral destruction of medial precentral cortex. Experiment one will directly examine whether spontaneous behavioral recovery, over the course of 4-6 weeks, is directly related to dopamine receptor mechanisms. Previous research has indicated that spontaneous behavioral recovery from neglect is correlated with changes in the behavioral response to administration of the dopamine receptor agonist, apomorphine. Subjects that have been allowed to spontaneously recover will be administered spiroperidol at one of five dosage levels. If spontaneous recovery is related to dopamine receptor mechanisms, then dopamine receptor blockade should reinstate neglect. It has been shown that 48 hours of light deprivation produces accelerated recovery of function. Experiment two will examine if this accelerated recovery is related to dopamine receptor mechanisms. If accelerated recovery is produced by the same receptor mechanisms as spontaneous recovery, then spiroperidol would be expected to reinstate neglect. Recent pharmacological findings in a human patient with neglect have indicated that the pharmacological data obtained in this rodent model generalized to human patient with chronic neglect. These findings suggest that pharmacological data relevant to the mechanisms of recovery of function obtained in the model will be relevant to the mechanisms of recovery of function from neglect in human patients.